Chemotherapy-induced executioner caspase activation increases breast cancer malignancy through epigenetic de-repression of CDH12.

ABSTRACT: Cancer relapse and metastasis are major obstacles for effective treatment. One important mechanism to eliminate cancer cells is to induce apoptosis. Activation of executioner caspases is the key step in apoptosis and was considered "a point of no return". However, in recent years, accumulating evidence has demonstrated that cells can survive executioner caspase activation in response to apoptotic stimuli through a process named anastasis. Here we show that breast cancer cells that have survived through anastasis (anastatic cells) after exposure to chemotherapeutic drugs acquire enhanced proliferation and migration. Mechanistically, cadherin 12 (CDH12) is persistently upregulated in anastatic cells and promotes breast cancer malignancy via activation of ERK and CREB. Moreover, we demonstrat

SUBMITTER: Wang Y 

PROVIDER: S-EPMC10290709 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature